Gypenoside XVII

Research use only, not for human use.

Gypenoside XVII confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, activation of Nrf2/ARE/HO-1 and inactivation of GSK-3β pathways.

Gypenoside XVII confers protection against Aβ25-35-induced neurotoxicity through estrogen receptor-dependent activation of PI3K/Akt pathways, activation of Nrf2/ARE/HO-1 and inactivation of GSK-3β pathways.

The ability of Gypenoside XVII (GP-17) to prevent Ox-LDL-induced cytotoxicity is detected by cell viability assays. Gypenoside XVII does not demonstrate any cytotoxicity in HUVECs.Gypenoside XVII can protect HUVECs against Ox-LDL-induced apoptosis.Gypenoside XVII dose-dependently mitigates the toxic effect of Ox-LDL on HUVEC viability.The viability of HUVECs is significantly higher than that of other groups at 50 μg/mL Gypenoside XVII .

Body weights are measured as physical measures of hormone bioactivity. Mean body weights are significantly higher in every group compared to that of the control, but there is no significant difference in body weight between the different treatments during the 10-week feeding. The mouse plasma lipid levels are also measured at the end of 10 weeks of a high-fat diet. Circulating levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) are significantly increased in the treated groups of ApoE-/- mice compared with those of the C57BL/6J control group; Gypenoside XVII (GP-17) and Probucol treatment substantially decreases both of these parameters relative to those of the ApoE-/- model group.

Gynosaponin S

Apoptosis

Caspase

GSK-3β

Others-Field

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80321-69-3

947.16

C48H82O18

>98% (HPLC)

DMSO : ≥ 100 mg/mL; 105.58 mM

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——

(-20℃)

With Ice Pack

≥ 2 years